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黏膜病的发病机制:一种由内部缺失产生的细胞病变性瘟病毒。

Pathogenesis of mucosal disease: a cytopathogenic pestivirus generated by an internal deletion.

作者信息

Tautz N, Thiel H J, Dubovi E J, Meyers G

机构信息

Federal Research Centre for Virus Diseases of Animals, Tübingen, Germany.

出版信息

J Virol. 1994 May;68(5):3289-97. doi: 10.1128/JVI.68.5.3289-3297.1994.

DOI:10.1128/JVI.68.5.3289-3297.1994
PMID:8151789
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC236819/
Abstract

Cytopathogenic bovine viral diarrhea virus (BVDV) arises by RNA recombination in animals persistently infected with noncytopathogenic BVDV. Such animals develop fatal mucosal disease. In this report, the genome of a cytopathogenic BVDV isolate, termed CP9, is characterized. CP9-infected cells contained not only viral genomic RNA of 12.3 kb but also a BVDV-specific RNA of 8 kb. cDNA cloning and sequencing revealed that the 8-kb RNA is a BVDV genome with an internal deletion of 4.3 kb. The 8-kb RNA represents the genome of a typical defective interfering particle (DI), since its replication was strictly dependent on the presence of a helper virus and strongly interfered with the replication of the helper. Cell culture experiments demonstrated that the CP9 virus stock contains two viruses, namely, a helper virus and DI9. While the helper virus alone was noncytopathogenic, the presence of the DI conferred cytopathogenicity. Expression experiments demonstrated that p80, the marker protein of cytopathogenic BVDV, is translated from the defective genome. The occurrence of this cytopathogenic DI is linked to a fatal disease in cattle.

摘要

细胞病变性牛病毒性腹泻病毒(BVDV)是由持续感染非细胞病变性BVDV的动物体内的RNA重组产生的。这类动物会发展为致命的黏膜病。在本报告中,对一种名为CP9的细胞病变性BVDV分离株的基因组进行了表征。感染CP9的细胞不仅含有12.3 kb的病毒基因组RNA,还含有8 kb的BVDV特异性RNA。cDNA克隆和测序显示,8 kb的RNA是一个内部缺失4.3 kb的BVDV基因组。8 kb的RNA代表典型缺陷干扰颗粒(DI)的基因组,因为其复制严格依赖于辅助病毒的存在,并强烈干扰辅助病毒的复制。细胞培养实验表明,CP9病毒株含有两种病毒,即辅助病毒和DI9。单独的辅助病毒无细胞病变性,但DI的存在赋予了细胞病变性。表达实验表明,细胞病变性BVDV的标记蛋白p80是由缺陷基因组翻译而来的。这种细胞病变性DI的出现与牛的一种致命疾病有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1a/236819/3966974521ca/jvirol00014-0530-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1a/236819/de4f082a3910/jvirol00014-0527-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1a/236819/a1609185923c/jvirol00014-0527-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1a/236819/8ab0c6dc71e4/jvirol00014-0529-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1a/236819/3966974521ca/jvirol00014-0530-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1a/236819/de4f082a3910/jvirol00014-0527-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1a/236819/a1609185923c/jvirol00014-0527-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1a/236819/8ab0c6dc71e4/jvirol00014-0529-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1a/236819/3966974521ca/jvirol00014-0530-a.jpg

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